XXII. BIOCHEMICKÝ ZJAZD - Jesseniova lekárska fakulta

Posters
94.
SELECTIve PHOSPHODIESTEraSE-3 INHIBITOr OLPrINONE aLLEviaTES
OXIDaTIve LUNG INJUry INDUCED BY MECONIUM
Daniela Mokrá 1 , Anna Drgová 2 , Rudolf Pullmann st. 3 and Andrea Čalkovská 1
1
Department of Physiology, 2 Department of Biochemistry, 3 Department of Clinical
Biochemistry, Jessenius Faculty of Medicine, Comenius University, Martin
In the pathophysiology of neonatal meconium aspiration syndrome, inflammation and
oxidation play a key role. This study evaluated effects of phosphodiesterase (PDE)-3
inhibitor olprinone on meconium-induced lung injury.
Oxygen-ventilated adult rabbits received intratracheally meconium or saline (Sal, n=7).
Thirty minutes after meconium instillation, animals were treated by olprinone (0.2 mg/kg
i.v., Mec+Olp, n=7) or were left without treatment (Mec, n=8). All animals were oxygenventilated
for additional 5 hours. Left lungs were saline-lavaged and differential WBC in
the sediment was estimated. Right lungs were used to determine lung edema by wet/
dry weight ratio and oxidative damage by estimation of thiol content, conjugated dienes,
thiobarbituric acid-reactive substances (TBARS), dityrosines and lysine-lipid peroxidation
products concentrations, cytochrome c oxidase activity (COX) in mitochondria of lung,
and total antioxidant status (TAS) in lung homogenate. In blood plasma, TBARS and TAS
were determined.
Meconium instillation increased lung neutrophils and edema formation and concentrations
of oxidation markers and decreased concentration of TAS. Olprinone reduced the lung
edema, lung neutrophils and several oxidation markers and increased TAS concentrations.
Selective PDE-3 inhibitor olprinone effectively reduced oxidative lung injury in meconiuminstilled
animals.
Acknowledgments: Supported by Project “Center of Excellency in Perinatology” No.
26220120016 co-financed by EC, and by Grant VEGA No. 1/0061/08.
218 XXII. Biochemistry Congress, Martin